The overall objective of the present research is to determine the molecular basis for resistance and susceptibility to larval schistosomes in genetically-defined stocks of the snail Biomphalaria glabrata. Ongoing research has been aimed at investigating (1) the ability of larval schistosomes to modulate their surface membranes during miracidial-sporocyst transformation by altering shared membane antigens or through antigenic masking, (2) antigenic sharing between snail hemocyte membrane determinants and miracidia, (3) hemocytopoeisis, and the activation of schistosome-reactive hemocytes, and (4) the effects of heterologous parasite infections (nematodes) on early schistosome development. Preliminary results indicate that antigens of early sporocyst membranes and snail hemocyte membranes may be crossreacting with anti-snail and ant-miricidium antibodies, respectively. Selective adsorption of snail serum components on to sporocyst surface membranes, however, could not be demonstrated with the antisera employed in these studies. An increase in circulating hemocytes, the result of 14C-thymidine injections, was apparently not the result of activated hemocytopoeisis, since autoradiographic analysis of hemocytes indicated no significant radiolabel incorporation. Finally, infection by nematdes (Daubaylia sp.) appear to cause a reduction in schistosome infectivity in susceptible snails. The nature of this suppression is unknown.